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MicroRNA-34a dependent regulation of AXL controls the activation of dendritic cells in inflammatory arthritis

Overview of attention for article published in Nature Communications, June 2017
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (87th percentile)
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

news
1 news outlet
twitter
7 tweeters
facebook
2 Facebook pages

Citations

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28 Dimensions

Readers on

mendeley
48 Mendeley
Title
MicroRNA-34a dependent regulation of AXL controls the activation of dendritic cells in inflammatory arthritis
Published in
Nature Communications, June 2017
DOI 10.1038/ncomms15877
Pubmed ID
Authors

Mariola Kurowska-Stolarska, Stefano Alivernini, Emma Garcia Melchor, Aziza Elmesmari, Barbara Tolusso, Clare Tange, Luca Petricca, Derek S. Gilchrist, Gabriele Di Sante, Chantal Keijzer, Lynn Stewart, Clara Di Mario, Vicky Morrison, James M. Brewer, Duncan Porter, Simon Milling, Ronald D. Baxter, David McCarey, Elisa Gremese, Greg Lemke, Gianfranco Ferraccioli, Charles McSharry, Iain B. McInnes

Abstract

Current treatments for rheumatoid arthritis (RA) do not reverse underlying aberrant immune function. A genetic predisposition to RA, such as HLA-DR4 positivity, indicates that dendritic cells (DC) are of crucial importance to pathogenesis by activating auto-reactive lymphocytes. Here we show that microRNA-34a provides homoeostatic control of CD1c(+) DC activation via regulation of tyrosine kinase receptor AXL, an important inhibitory DC auto-regulator. This pathway is aberrant in CD1c(+) DCs from patients with RA, with upregulation of miR-34a and lower levels of AXL compared to DC from healthy donors. Production of pro-inflammatory cytokines is reduced by ex vivo gene-silencing of miR-34a. miR-34a-deficient mice are resistant to collagen-induced arthritis and interaction of DCs and T cells from these mice are reduced and do not support the development of Th17 cells in vivo. Our findings therefore show that miR-34a is an epigenetic regulator of DC function that may contribute to RA.

Twitter Demographics

The data shown below were collected from the profiles of 7 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 48 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 48 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 13 27%
Researcher 8 17%
Unspecified 6 13%
Student > Postgraduate 5 10%
Student > Master 5 10%
Other 11 23%
Readers by discipline Count As %
Medicine and Dentistry 11 23%
Agricultural and Biological Sciences 9 19%
Unspecified 8 17%
Biochemistry, Genetics and Molecular Biology 7 15%
Immunology and Microbiology 6 13%
Other 7 15%

Attention Score in Context

This research output has an Altmetric Attention Score of 15. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 15 April 2018.
All research outputs
#960,362
of 12,801,967 outputs
Outputs from Nature Communications
#10,236
of 21,816 outputs
Outputs of similar age
#33,939
of 264,192 outputs
Outputs of similar age from Nature Communications
#540
of 975 outputs
Altmetric has tracked 12,801,967 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 92nd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 21,816 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 47.1. This one has gotten more attention than average, scoring higher than 53% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 264,192 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 87% of its contemporaries.
We're also able to compare this research output to 975 others from the same source and published within six weeks on either side of this one. This one is in the 44th percentile – i.e., 44% of its contemporaries scored the same or lower than it.